The objectives of this research will be to determine whether or not there exists a physiological or pathological instance where the control of antidiuretic hormone (ADH) is influenced by the renin-angiotensin system. This will be studied in the dog by removing the angiotensin II stimulation from the composite of inputs normally converting enzyme inhibitor during situations of physiologically and/or pathologically elevated plasma renin activity (PRA). PRA will be elevated by dehydration, low Na ion diet, and constriction of the renal artery. In addition, whether or not circulating angiotensin II affects ADH release by acting on the brain will be investigated, as well as the effects of aldosterone on ADH release.